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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence, prognosis and causes of strokes associated with pregnancy or puerperium are poorly known, and we do not know whether and to what extent they differ from those of the general female population of childbearing age. Based on early and mostly hospital-based studies, it has been claimed that pregnancy increases the likelihood of cerebral infarction to about 13 times the rate expected outside of pregnancy. However, because of methodological weaknesses, these estimates must be regarded with caution. In a recent study in Ile de France, the incidence of arterial ischemic strokes associated with pregnancy or early puerperium was 4.3 per 100,000 deliveries (95% confidence interval, 2.4 to 7.1), a rate not much different from that for all women of childbearing age. Ischemic strokes related to various etiologies have been reported in pregnancy and the puerperium. Their relative frequency is poorly known because there are no recent large series of pregnancy-related ischemic strokes benefiting from detailed investigation with modern imaging techniques. Most of the known causes of ischemic stroke in the young been reported during pregnancy. In most of these conditions, it is uncertain whether pregnancy is coincidental or plays a role in the occurrence of stroke. Among pregnancy-specific causes, eclampsia may be associated with focal neurological deficits of sudden onset, consistent with a clinical diagnosis of stroke. However, the precise pathogenesis of these stroke-like focal deficits remains poorly understood. Except for some women who have persisting neurological deficits and neuroradiological abnormalities suggesting brain infarction, the reversibility of the neurological clinical signs and neuroradiological lesions within a few days or weeks in most cases argues against the existence of true cerebral ischemic necrosis. The two other pregnancy-specific causes-choriocarcinoma and amniotic fluid embolism-are rarely responsible for focal cerebral ischemia. Other diseases such as peripartum cardiomyopathy and postpartum cerebral angiopathy were initially considered as pregnancy-specific causes but subsequently reported outside of pregnancy. In a significant number of patients, the cause of the stroke remains undetermined, despite an extensive etiological workup. Whether hypercoagulable state and vessel wall changes associated with pregnancy may play a role in the occurrence of these otherwise unexplained ischemic strokes remains unknown. Too frequently, the stroke is considered at the first attempt as a complication of pregnancy and another underlying etiology may be missed. Therefore, evaluation of arterial ischemic stroke in pregnancy should proceed as in the non-pregnant state. There are no follow-up studies that consider the risk of recurrent stroke in future pregnancies. No data are available on the risk associated with use of oral contraception in a woman who had ischemic stroke during pregnancy. The frequency of cerebral venous thrombosis associated with pregnancy and the puerperium is not precisely known. Indeed, epidemiologic studies have been difficult to perform because cerebral venous thrombosis may have a misleading presentation and a definite diagnosis requires angiography, MRI or autopsy. The incidence of cerebral venous thrombosis has been estimated at 10 to 20 per 100000 deliveries in occidental countries, whereas rates of 200 to 500 per 100,000 deliveries have been reported in India. The pregnant and puerperal state accounts for 5 to 20% of all cerebral venous thrombosis in occidental countries; this proportion may reach 60% in developing countries. Labor and delivery are characteristically normal in occidental countries. The occurrence of cerebral venous thrombosis is clearly linked to the puerperial state, suggesting a direct role of the puerperial state.(ABSTRACT TRUNCATED)
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PMID:[Cerebrovascular diseases in pregnancy and puerperium]. 894 39

Physiological changes occurring during pregnancy and puerperium may increase the risk of stroke. However, the incidence rate of ischemic stroke is of 3.8 to 5 in 100,000 pregnancies, i.e. quite similar to that of ischemic strokes occurring in non pregnant women of child bearing age. Whereas eclampsia, choriocarcinoma and amniotic emboli occur only during pregnancy or puerperium, peripartum cardiomyopathy and benign cerebral angiopathy are less specific. All other causes of cerebral ischemia may also occur during pregnancy and puerperium. The management of an ischemic stroke should not differ between pregnant and non pregnant women of child bearing age. Strokes associated with pregnancy require a complete diagnostic work-up including angiography if necessary. Low doses of aspirin (60-80 mg/d) can be used after 3 months of pregnancy. Heparin is the anticoagulant of choice during pregnancy, but warfarin may be used between 13 and 36 weeks of gestation; heparin and warfarin can be used during breast feeding. There is no neurological reason to recommend a systematic use of cesarean section. Subsequent prescription of oral contraceptive therapy is not recommended except in patients with a definite cause of ischemic stroke which is not influenced by hormones.
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PMID:Arterial ischemic strokes associated with pregnancy and puerperium. 910 39

Following cerebral ischaemia a recurrent stroke must be avoided in most patients by means of antithrombotic agents. Based on the results reviewed here of new therapy studies, we discuss the presently available antithrombotic treatment options for prophylaxis in ischaemic stroke. TASS (Ticlopidine Aspirin Stroke Study) and CATS (Canadian American Ticlopidine Study) are two multicentre studies investigating the effect of ticlopidine, a new antiplatelet agent of the thienopyridine family, compared to acetylsalicylic acid (ASA) respectively placebo, in the secondary prophylaxis of ischaemic stroke. A significant relative risk reduction of ticlopidine against ASA (21%) and against placebo (28.1%) was shown. CAPRIE (Clopidogrel vs. Aspirin in Patients with Risk of Ischemic Events) evaluated clopidogrel and ASA in the secondary prophylaxe of stroke, myocardial infarction and peripheral vascular occlusive disease. Clopidogrel has been shown to be as effective as ticlopidine compared to ASA in the secondary prevention of vascular disease but had the advantage of a far less severe side effect profile as ticlopidine. ESPS 2 (2nd European Stroke Prevention Study) compared dipyridamole and ASA alone and in combination against placebo in stroke prevention. The combination of agents showed a 24.4% relative risk reduction to suffer ischaemic stroke as opposed to placebo. The ranking of heparin and heparinoids in the secondary prevention of ischaemic stroke has not been completely established but seems to diminish according to recently published data from three major trials. The American TOAST study (Trial of Org 10172 in Acute Stroke Treatment) failed to prove any advantage of intravenous Orgaran compared to placebo. In IST (International Stroke Trial) and CAST (Chinese Acute Stroke Trial) the benefits of heparin are invalidated by a higher bleeding rate of patients on intravenous heparin therapy. Furthermore, the results of IST have to be judged critically because of significant methodical inadequacies. When applying antithrombotic agents, therapeutic effect and presumed better outcome should be weighed against the risk of associated bleedings. The indication for an antithrombotic treatment should be reevaluated in regular control examinations and the possibility of a less aggressive treatment should be considered.
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PMID:[Antithrombotic therapy after cerebral ischemia]. 941 27

The study of the cerebral white matter (WM) in experimental models of hypoxia and ischemia has been for a long time neglected, the interest of investigators being focused on the response of the neuronal population. The increasing frequency with which modern neuroimaging techniques disclose alterations of the WM of possibly vascular origin has called some attention to other components of the cerebral parenchyma, namely oligodendrocytes and myelinated axons. The studies here reviewed show that it is possible to investigate the WM alterations in appropriate models of cerebral ischemia. In rodents, chronic ischemia produces extracellular fluid accumulation in the WM, moderate loss of oligodendroglial cells and reactive astrogliosis, all of which contribute to the rarefied appearance under the light microscope. These changes are similar to those found in many patients with leukoencephalopathy of possibly vascular origin. The results of experiments using a rat model of focal brain ischemia show that oligodendrocytes and myelinated fibers are extremely sensitive to ischemic insults with alterations of the subcortical WM detected at a very early time. Opportune modifications of these animal models may represent a valuable source of information on the pathogenesis and pathophysiology of human vascular disease of the WM.
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PMID:Experimental approaches to white matter disease. 971 40

Modeling of focal cerebral ischemia seeks to understand mechanisms of injury and to test agents as potential stroke therapies. However, modeling has been singularly unpredictable in ischemic cerebrovascular disease for a number of reasons related to the incompletely understood pathophysiology of ischemic stroke and to the characteristics of models prepared to mimic the clinical condition. The development of models of focal cerebral ischemia must take into account known species differences and idiosyncrasies, underlying vascular disease processes, the nature of thrombotic processes, cellular reactivities, the presence of co-stimulation (e.g., inflammation), the characteristics of immunologicals and reporter molecules, the coincident use of other pharmacologic modifiers (e.g., anesthesia), and stress. These elements are also potential contributors to cerebral tissue injury and its assessment but may affect other species differentially. On the other hand, study design issues have been shown to be particularly relevant to limiting development of some agents for clinical stroke treatment. Experience from experimental and clinical work on vascular active approaches (e.g., plasminogen activators) suggests that active dialogue regarding the relationships between clinical outcomes and outcomes in appropriate animal models is necessary. Success appears more likely when the model more closely matches the known human pathophysiology and the interventions applied in the models are definitely characterized in that species. Rather than moving directly to interventional studies in humans, the use of several appropriate animal models is encouraged where those models exist. Where not, careful consideration of study design and the biology of the disorder is a prerequisite.
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PMID:Clinical trials in acute stroke: why have they not been successful? 974 38

The effect of Ginkgo biloba extract (GbE) on cerebral ischemia induced by 10-min bilateral occlusion of the carotid arteries in mice was studied. Severe impairment of memory was apparent when the passive avoidance test was carried out 48 hr after bilaterally induced ischemia. When GbE at doses of 50 and 100 mg/kg was given p.o. 1 hr before the 10-min occlusion, there was a significant improvement in memory. The i.p. injection of ifenprodil (30 mg/kg) also showed improvement on learning tasks. The p.o. administration of flavonoid, a fraction isolated from GbE, showed high step-through latency on scopolamine-induced amnesia. All these findings indicate that GbE is beneficial for clinical use in amnesia accompanied with cerebral vascular disease.
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PMID:Effects of ginkgo biloba extract on impairment of learning induced by cerebral ischemia in mice. 979 64

Laser-scanning confocal microscopy (LSCM) was used to measure at high resolution cerebral plasma volumes (perfusion) using two fluorescent plasma markers in a rat model of embolic stroke. This application of LSCM to study the microvascular circulation in embolic stroke was developed as an alternative to autoradiography to measure cerebral perfusion. An additional benefit of LSCM is that it quantitates with great accuracy the structural relationships of the microcirculation to cells and the pathological alterations of the ischemic brain. Autoradiography allows only a quantitative analysis of cerebral perfusion. For example, in order to study the microcirculation and its relationship to blood brain barrier damage, the volume of perfused cerebral capillaries was measured by administering two fluorescent plasma markers (FITC-dextran and Evans blue) intravenously to a rat. Evans blue was administered before cerebral ischemia and FITC-dextran administered post-ischemia 1 min before sacrifice. Volumes of plasma perfusion were analyzed by means of a system developed for 3D analysis of fixed and stained serial brain histologies. Plasma volumes for the non-ischemic cerebral cortex were 1.00%+/-0.38% while plasma volumes in the caudate/putamen were 0.69%+/-0.17% in good agreement with the previously published values using the autoradiography method. The architecture of the capillaries in the ischemic core showed perfusion of Evans blue but there was no flow of FITC dextran. Our work represents a novel application of this technology to investigation of cerebral vascular disease and identifies its potential to become an important tool for investigation of cerebral pathology.
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PMID:High resolution quantitation of microvascular plasma perfusion in non-ischemic and ischemic rat brain by laser-scanning confocal microscopy. 1044 13

Intracerebral hemorrhage is a common cause of acute neurological deterioration and a frequent indication for emergency neuroimaging. Stroke symptoms are caused in 10 to 15% by intracerebral hemorrhage. It is often not possible to differentiate intracerebral hemorrhage from cerebral ischemia by clinical examination. The therapeutic decision between thrombolysis or conservative therapy is comprised by the etiology. To exclude intracerebral hemorrhage as the cause of clinical symptoms, a CT is usually performed. Localisation and extension of the acute intracerebral hemorrhage are easy to detect. Subacute and chronic intracerebral hemorrhage are better delineated with magnetic resonance imaging. The different signal of the hemorrhage can be used for the age of the intracerebral hemorrhage. The cause of a non-traumatic intracerebral hemorrhage is in over 60% hypertony, less frequent alcoholism, malformation, or amyloid angiopathy. Uncommon causes of hemorrhage are head trauma, blood dyscrasia, tumor or venous thrombosis. Non-traumatic intracerebral hemorrhage are most common in patients between 50 and 70 years. In younger patients a malformation should be excluded with a cerebral angiography. Intracerebral hemorrhages are usually conservatively treated, in some cases an operative decompression is performed.
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PMID:[Spontaneous intracerebral hemorrhage: the clinical neuroradiological view]. 1055 Mar 81

The chronic stage of vasospasm occurring several days after subarachnoid hemorrhage (SAH) is characterized by the development of histopathologic changes in cerebral arteries causing cerebral ischemia. Numerous experimental data indicate the involvement of immune mechanisms in the angiopathy caused by SAH. Endogenous opioids play also an important role in the ischemic lesions of the brain. Corticotropin releasing hormone (CRH) induces the release of beta-endorphin (beta-END) from hypothalamic neurons and also from mononuclear white blood cells. The function of CRH and beta-END in vasospasm following SAH and the interrelationship between neuroendocrine and immune changes requires further elucidation. In the present study we investigated the influence of CRH injected into cerebral cisterna magna (CM) of rats on beta-END-like level in cerebrospinal fluid (CSF) in acute and chronic phase of cerebral vasospasm following artificial SAH. Acutely CRH induced a significant rise of beta-END-like in CSF both in SAH and sham SAH rats. However, in rats subjected to SAH, a single injection of CRH caused a prolonged rise of 5-END in CSF, which was also seen 2 days after SAH, during the chronic phase of vasospasm. The obtained results indicate that CRH increases neuroendocrine changes induced by SAH, probably by an activation of immune cells involved in the patomechanism of chronic vasospasm.
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PMID:Corticotropin releasing hormone (CRH) increases beta-endorphin (beta-end like) concentration in cerebrospinal fluid of rats with vasospasm following subarachnoid hemorrhage. 1057 71

Cerebral ischemia is an important cerebral vascular disease, and zinc is a necessary trace element for humans. In this work, a cerebral ischemia model of rabbit was established by operation. The samples of brain and serum in the animal models were collected. The Zn contents in the samples were determined by neutron activation analysis and inductively coupled plasma-atomic emission spectrometry. The results show the Zn contents in brain decreased 2 mo after cerebral ischemia, and Zn contents in serum decreased even more obviously. In addition, a positive correlation of Zn contents between left and right cerebral hemispheres was observed, and the positive correlation between brain and serum was also observed. A test of Chinese medicine was also carried out in the work. Two Chinese medicines were fed to rabbits with cerebral ischemia in the experiments. The results showed they probably can prevent the decrease of Zn contents in serum.
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PMID:Determination of zinc contents in rabbits with cerebral ischemia by NAA and ICP-AES. 1067 39


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